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Role of fibroblast growth factor-23 in renal disease activity and bone density involvement in patients with lupus
Nashwa M Azoz1, Ammar A Ammar1, Howaida A Nafady2
1Internal Medicine-Nephrology Division, Assiut University Hospital, Faculty of Medicine, Assiut University, Assiut 71711, Egypt.
Background:
Systemic lupus erythematosus-associated lupus nephritis (LN) represents a major contributor to disease-related morbidity. Disturbances in bone metabolism frequently coexist with LN, driven in part by persistent inflammation and impaired renal function. These factors are closely linked to decreased bone mineral density (BMD) and a heightened risk of fractures. Fibroblast growth factor-23 (FGF-23) has recently been recognized as a key regulator of mineral homeostasis and may serve as a marker reflecting both renal disease activity and skeletal involvement. Nevertheless, its precise role in LN activity and its impact on bone health remain inadequately defined.
Aim:
To determine the predictive value of FGF-23 in renal disease activity and bone density changes in patients with LN.
Methods:
A cross-sectional hospital-based study included 100 adult patients with LN. Patients were classified into active (n = 50) and inactive LN (n = 50). All patients underwent clinical assessment, laboratory investigations, renal imaging, renal biopsy when indicated, and BMD assessment using dual-energy X-ray absorptiometry. Serum FGF-23 was measured using enzyme-linked immunosorbent assay. Statistical analysis included comparative tests, correlation analysis, logistic regression, and receiver operating characteristic curve analysis.
Results:
Patients with active LN had significantly higher FGF-23 levels compared with those with inactive LN (149.44 ± 37.09 pg/mL vs 122.56 ± 36.91 pg/mL; P < 0.001). BMD was significantly lower in patients with active LN (0.42 ± 0.19 g/cm² vs 0.56 ± 0.16 g/cm²; P < 0.001), with low BMD observed in 80% of patients with active LN vs 26% of those with inactive LN. FGF-23 level showed a significant negative correlation with BMD (r = -0.67, P = 0.001). Elevated FGF-23 level independently predicted low BMD (odds ratio = 4.18) and active LN (odds ratio = 2.18). At a cut-off point of ≥ 135 pg/mL, FGF-23 predicted low BMD with 79.5% accuracy.
Conclusion:
FGF-23 may be a promising biomarker for renal disease activity and BMD in patients with LN. Its elevation may reflect the interplay between disturbances in mineral metabolism, inflammatory processes, and renal involvement. Nevertheless, further large-scale, longitudinal studies are required to validate these observations and clarify the clinical utility of FGF-23 in patients with LN.
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